@article {Pomara:2015:1570-159X:132,
title = "Neurotoxicity by Synthetic Androgen Steroids: Oxidative Stress, Apoptosis, and Neuropathology: A Review",
journal = "Current Neuropharmacology",
parent_itemid = "infobike://ben/cn",
publishercode ="ben",
year = "2015",
volume = "13",
number = "1",
publication date ="2015-01-01T00:00:00",
pages = "132-145",
itemtype = "ARTICLE",
issn = "1570-159X",
url = "https://www.ingentaconnect.com/content/ben/cn/2015/00000013/00000001/art00013",
keyword = "neuroprotective strategies, Androgen-anabolic steroids, neurotoxicity, excitotoxic neuronal death, neurotrophin
unbalance, apoptosis, oxidative-stress, biochemical mechanisms",
author = "Pomara, Cristoforo and Neri, Margherita and Bello, Stefania and Fiore, Carmela and Riezzo, Irene and Turillazzi, Emanuela",
abstract = "Anabolic-androgenic steroids (AAS) are synthetic substances derived from testosterone that are largely employed due to their trophic effect on muscle tissue of athletes at all levels. Since a great number of organs and systems are a target of AAS, their adverse effects are primarily
on the following systems: reproductive, hepatic, musculoskeletal, endocrine, renal, immunological, infectious, cardiovascular, cerebrovascular, and hematological. Neuropsychiatric and behavioral effects as a result of AAS abuse are well known and described in the literature. Mounting evidence
exists suggesting that in addition to psychiatric and behavioral effects, non-medical use of AAS carries neurodegenerative potential. Although, the nature of this association remains largely unexplored, recent animal studies have shown the recurrence of this AAS effect, ranging from neurotrophin
unbalance to increased neuronal susceptibility to apoptotic stimuli. Experimental and animal studies strongly suggest that apoptotic mechanisms are at least in part involved in AAS-induced neurotoxicity. Furthermore, a great body of evidence is emerging suggesting that increased susceptibility
to cellular oxidative stress could play a pivotal role in the pathogenesis of many neurodegenerative disorders and cognitive impairment. As in other drug-evoked encephalopathies, the key mechanisms involved in AAS induced neuropathology could represent a target for future neuroprotective
strategies. Progress in the understanding of these mechanisms will provide important insights into the complex pathophysiology of AAS-induced neurodegeneration, and will pave the way for forthcoming studies. Supplementary to abandoning the drug abuse that represents the first step in reducing
the possibility of irreversible brain damage in AAS abusers, neuroprotective strategies have to be developed and implemented in future.",
}